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Phyto 
Health Clinic

Natural Health Clinic London - Natural Endocrine Clinic

Endocrinology is the study of diseases caused by hormonal dysfunction. We investigate and help in the management of all common endocrine disorders including metabolism, lipoprotein, obesity and thyroid disease.

Facilities include dynamic testing and Nutrition advice for

  • Diabetes
  • Obesity
  • Hypothyroidism
  • Hyperthyroidism

Thyroid disease, responsible for a spectrum of pathology from subclinical hormonal abnormalities to life-threatening disease, is easily and effectively treated. Between 5.9% and 11.7% of the population has abnormal values on thyroid screening. Hypothyroidism is 5 to 10 times as prevalent as thyrotoxicosis; symptomatic disease is found in 5% to 10% of patients with abnormal laboratory values. Thyrotoxic patients more commonly manifest clinical symptoms.

Thyroid Physiology

Thyroid-stimulating hormone (TSH), secreted by the anterior pituitary gland, controls the synthesis and secretion of the thyroid hormones, thyroxine (T4) and triiodothyronine (T3). Regulation of TSH levels is controlled by two mechanisms. The first is classic negative feedback to serum thyroid hormone concentration. Large inverse changes in TSH levels are precipitated by small changes in free thyroid hormone concentrations. Secondly, TSH concentration is regulated by the hypothalamic hormone thyrotropin-releasing hormone (TRH). The systems are interrelated in that the negative feedback of thyroid hormone probably affects TRH release from the hypothalamus in addition to TSH release from the pituitary. Thyroid-releasing hormone secretion is also affected by input from higher cortical centers. This system of thyroid hormone production is referred to as the hypothalamic-pituitary-thyroid axis.

At the molecular level, T4 is actually a prohormone and T3 is the biologically active chemical. All T4 is synthesized within the thyroid gland, whereas only 15% to 20% of T3 is synthesized directly. T4 is converted to T3 in peripheral organs, including the kidneys and liver. Thyroglobulin is a thyroid-hormone-containing protein stored in the colloid within thyroid follicles. T4 synthesis occurs within these follicles. Dietary iodide is trapped, oxidized, and combined with tyrosine residues. Coupling of these iodotyrosines produces T4. In healthy patients, about 41% of T4 is metabolized to T3 and 38% converts to RT3.

The daily requirement for thyroid hormone is less than 1% of the amount stored within the gland, allowing maintenance of normal function when a person is deprived of iodine. The excess capacity, however, creates a vulnerability to thyrotoxicosis when the thyroid gland becomes inflamed and excess thyroid hormone is released.

Free T3 (FT3) and free T4 (FT4) serum levels provide more valuable clinical information. Thyroid-stimulating hormone secretion rhythmically varies between day and night. More than half is secreted in pulsatile fashion between 10:00 p.m. and 4:00 a.m. Sleep deprivation increases pulses, whereas sleep diminishes the pulses. The TSH molecules secreted at night demonstrate less hormonal activity than do daytime molecules. Therefore, there is no nocturnal surge in thyroid hormone levels in response to the increased secretion of TSH.

Hypothyroidism

The term hypothyroidism encompasses a broad spectrum of disease. Hypothyroidism can be congenital or acquired, primary or secondary, overt or subclinical, and goiterous or nongoiterous. Primary hypothyroidism, caused by thyroid gland failure, is responsible for more than 95% of cases of hypothyroidism. Low TSH or TRH levels from pituitary or hypothalamic failure cause central hypothyroidism, a relatively rare condition.

In areas of the world where iodine deficiency is unusual, most cases of primary hypothyroidism are associated with Hashimoto’s thyroiditis. Also known as chronic autoimmune thyroiditis, this disease is characterized by lymphocytic infiltration of the thyroid gland and the presence of antibodies directed against the TSH receptor, thyroperoxidase (TPO), and thyroglobulin. The TSH-receptor antibodies target a different area of the receptor than those found in patients with Grave’s disease; these antibodies block the action of TSH rather than stimulate the gland. Seven of 10 patients with Hashimoto’s thyroiditis are women, and the incidence increases with age. The disease assumes goiterous and atrophic forms; patients with goiter are usually asymptomatic but sometimes have thyroid tenderness not responsive to steroids.

Less common causes of hypothyroidism are listed in the tables below. The initial thyrotoxicosis seen in thyroiditis is often followed by a period of transient hypothyroidism. Iodine deficiency is the most common cause of hypothyroidism and goiter worldwide; it is rare in the United States due to the iodination of table salt. Paradoxically, iodine excess can also cause hypothyroidism: it inhibits the organification of iodine and the synthesis of T3 and T4 (the Wolff-Chaikoff effect).

 

Differential Diagnosis of Hypothyroidism


Mechanisms

TSH

FT4, FT3

Primary hypothyroidism




Hashimoto’s disease

Autoimmune disease

High

Low

Surgical thyroidectomy

Iatrogenic

High

Low

External radiation

Iatrogenic

High

Low

Amyloidosis

Infiltrative

High

Low

Lymphoma

Infiltrative

High

Low

Scleroderma

Infiltrative

High

Low

Iodine deficiency or excess

Nutritional

High

Low

Drug-induced

Iatrogenic

High

Low

Secondary hypothyroidism




Sheehan’s Syndrome

Pituitary infarction

Low

Low

Pituitary neoplasm

Infiltrative/malignant

Low

Low

Pituitary radiation/surgery

Iatrogenic

Low

Low

Tertiary hypothyroidism




Sarcoidosis

Hypothalamic infiltration

Low

Low

Hypothalmic neoplasm

Malignancy

Low

Low

Clinical manifestations of hypothyroidism are the consequence of two basic physiologic effects of the lack of thyroid hormone: generalized slowing of metabolic processes and tissue deposition of glycosaminoglycans. Clinical manifestations of hypothyroidism with relative frequencies are listed in the following table. Because signs and symptoms of hypothyroidism are often nonspecific, develop insidiously, and can be mistaken for normal aging, clinical detection can be difficult. Accordingly, laboratory testing has assumed an increasingly important role in the detection of hypothyroidism.

 

Sensitivity and Specificity of the 14 Symptoms and Signs of Hypothyroidism

Symptoms/Signs

Sensitivity (%)

Specificity (%)

Ankle reflex

77

93.5

Dry skin

76

63.8

Cold intolerance

64

65

Coarse skin

60

81.2

Puffiness

60

96.3

Pulse rate < 75/mina

58

42.5

Diminished sweating

54

86.2

Weight increase

54

77.5

Paraesthesia

52

82.5

Cold skin

50

80

Constipation

48

85

Slow movements

36

98.7

Hoarseness

34

87.5

Hearing impairment

22

97.5

Myxedema coma is a rare and potentially lethal complication of hypothyroidism. It is usually the result of acute decompensation in a patient with chronic hypothyroidism, often precipitated by stress such as infection, cold exposure, trauma, surgery, or stroke or the use of medications such as amiodorone and lithium. The condition is seen almost exclusively in women over 60 years of age and usually occurs during winter months. Contrary to the name, patients do not necessarily present with coma or oedema; clinical findings can include altered mental status, hypothermia, hypoventilation, hypotension, bradycardia, constipation, periorbital edema, nonpitting peripheral edema, and delayed relaxation of deep tendon reflexes. Associated abnormal laboratory findings can include anemia, hyponatremia, hypoglycemia, and elevated total creatinine kinase (CPK) levels. Myxedema coma can result in cardiovascular collapse; prompt recognition and treatment can be life saving.

 

Thyrotoxicosis and Hyperthyroidism

Thyrotoxicosis refers to the increased metabolic and sympathetic nervous state that develops when serum concentrations of free thyroid hormone are elevated. One effect is increased sensitization to catecholamines. The terms thyrotoxicosis and hyperthyroidism are not synonymous. Hyperthyroidism, defined as thyroid gland hyperfunction, causes thyrotoxicosis due to increased thyroid hormone biosynthesis and release. Increased levels of thyroid hormone can occur, however, when thyroid gland function is normal. Examples include excess release of stored hormone from thyroid gland inflammation, excess exogenous thyroid hormone ingestion, and production of thyroid hormone from ectopic foci. Careful clinical evaluation complemented by appropriate laboratory investigation can clarify the specific aetiology of thyrotoxicosis.

Graves’ disease is the most common cause of hyperthyroidism in middle-aged patients and is the aetiology for 60% to 80% of all hyperthyroid patients. It is autoimmune in origin. Anti-TSH antibodies cause hyperstimulation of thyroid hormone and thyroid follicle hyperplasia. On physical examination, goiter, exophthalmos, and pretibial myxedema constitute the classic triad of Graves’ disease. Other causes of hyperthyroidism are listed below.

 

Differential Diagnosis of Thyrotoxicosis


Mechanisms

RAI Uptake

TSH

FT4, FT3

Hyperthyroid etiologies





Graves’ disease

TSH receptor antibodies    High

High

Low

High

Toxic multinodular goiter

Multiple foci of autonomous thyroid function

High

Low

High

Toxic adenoma

Benign thyroid tumor with autonomous function

High

Low

High

Molar pregnancy

Greatly increased HCG levels stimulate TSH receptors

High

Low

High

Pituitary tumor

TSH hypersecretion

High

High

High

Pituitary resistance to thyroid hormone

Failure of normal feedback mechanism

High

High

High

Nonhyperthyroid etiologies





DeQuervain’s thyroiditis

Release of stored hormone

Low

Low

High

Postpartum thyroiditis

Release of stored hormone

Low

Low

High

Lingual goiter

Ectopic thyroid hormone secretion

Low

Low

High

Struma ovarii

Ectopic thyroid hormone secretion

Low

Low

High

Thyroid carcinoma

Ectopic thyroid hormone secretion

Low

Low

High

Jod-Basedow phenomenon

Iodine exposure secondary to radiologic studies

Low

Low

High

Chronic amiodarone use

Iodine exposure from amiodarone

Low

Low

High

Thyrotoxicosis facititia

Intentional thyroid hormone ingestion

Low

Low

High

Iatrogenic thyrotoxicosis

Excessive dose of thyroid hormone supplement

Low

Low

High

Patients with thyrotoxicosis without hyperthyroidism may present initially to the ED. Subacute or de Quervain’s thyroiditis classically presents with a tender thyroid gland, tachycardia, and flu-like symptoms. Multiple viruses have been linked to the disease. Physical examination reveals a tender and enlarged thyroid gland. The illness is self-limited and may be treated symptomatically with aspirin. More severe symptoms respond to prednisone. Beta blockers may be used to treat peripheral manifestations of thyrotoxicosis.

Subacute painless thyroiditis occurs in 2% to 6% of postpartum women in the United States. The usual time course is 3 to 6 months after delivery. It is likely the result of rebound immune activity. Fifty percent of patients manifest a firm painless goiter on physical examination. Thyrotoxic symptoms persist from 1 to 3 months. Beta blockade is effective symptomatic therapy . Clinical manifestations are precipitated by excessive release of thyroid hormone. Thyroiditis, a non-hyperthyroid condition, is differentiated from thyroid gland hyperfunction by measurement of radioactive iodine (RAI) uptake. Patients with hyperthyroidism will have high RAI uptake due to the increased glandular activity. Those with thyroiditis or exogenous thyroid ingestion will have low RAI uptake in the face of thyrotoxicosis.

Clinical Manifestations of Thyrotoxicosis

Organ System

Symptoms

Physical Findings

Cardiovascular

Palpitations

Sinus tachycardia


Dyspnea

Atrial fibrillation



Congestive heart failure

Dermatologic

Hair loss

Hair loss



Warm, moist, smooth skin



Palmar erythema



Pretibial myxedema Onycholysis

Gastrointestinal

Increased appetite



Weight loss



Hyperdefecation



Diarrhea


Gynecologic

Oligomenorrhea



Amenorrhea



Symptoms following pregnancy


Neuropsychiatric

Anxiety

Fine tremor


Fatigue

Hyperreflexia


Insomnia

Muscle wasting and weakness


Irritability

Periodic paralysis


Heat intolerance


Ophthalmologic

Feeling of grittiness

Exophthalmos


Retrobulbar pressure

Conjunctival injection


Diplopia

Ophthalmoplegia

Thyroid gland

Neck fullness

Thyroid enlargement


Dysphagia


Reference
Thyroid disease in the emergency department: A clinical and laboratory review Journal of Emergency Medicine, Volume 28, Issue 2, February 2005, Pages 201-209 Laura Pimentel and Karen N. Hansen.